Results 111 to 120 of about 37,064 (267)

Mutant Huntingtin Forms in Vivo Complexes with Distinct Context-Dependent Conformations of the Polyglutamine Segment

open access: yesNeurobiology of Disease, 1999
Huntington's disease (HD) is caused by an expanded glutamine tract, which confers a novel aggregation-promoting property on the 350-kDa huntingtin protein.
Francesca Persichetti   +6 more
doaj   +1 more source

IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosome [PDF]

open access: yes, 2009
Expansion of the polyglutamine repeat within the protein Huntingtin (Htt) causes Huntington's disease, a neurodegenerative disease associated with aging and the accumulation of mutant Htt in diseased neurons.
Aiken   +97 more
core   +3 more sources

Exploring and Targeting the Connection of Iron and Copper Homeostasis to Neurodegenerative Diseases

open access: yesMedComm, Volume 7, Issue 6, June 2026.
Iron and copper dyshomeostasis, along with their interactions with key intrinsically disordered proteins (e.g., Aβ, tau, α‐synuclein) have a strong implication in the onset and progression of neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), Prion diseases (PrDs), Huntington's disease (HD), Wilson's disease (WD),
Xin Liu   +9 more
wiley   +1 more source

Reduced Levels of Proteasome Products in a Mouse Striatal Cell Model of Huntington's Disease.

open access: yesPLoS ONE, 2015
Huntington's disease is the result of a long polyglutamine tract in the gene encoding huntingtin protein, which in turn causes a large number of cellular changes and ultimately results in neurodegeneration of striatal neurons. Although many theories have
Sayani Dasgupta   +6 more
doaj   +1 more source

Multiple discrete soluble aggregates influence polyglutamine toxicity in a Huntington\u27s disease model system [PDF]

open access: yes, 2016
Huntington’s disease (HD) results from expansions of polyglutamine stretches (polyQ) in the huntingtin protein (Htt) that promote protein aggregation, neurodegeneration, and death.
Denis, Clyde L., Wang, Xin, Xi, Wen
core   +1 more source

Huntington's disease is a multi-system disorder. [PDF]

open access: yes, 2015
Huntingtons disease (HD) is one of the most common non-curable rare diseases and is characterized by choreic movements, psychiatric symptoms, and slowly progressive dementia.
Mielcarek, M
core   +1 more source

Cilia in Nervous System Development, Function, and Disease

open access: yesMedComm – Future Medicine, Volume 5, Issue 2, June 2026.
Cilia are evolutionarily conserved organelles that function as essential sensory and motility platforms in the nervous system. This review outlines key cilia‐dependent signaling pathways and their roles in neural development and function. Furthermore, it highlights how ciliary dysfunction can lead to a variety of neurological disorders, known as ...
Qingchao Li, Anqi Zhang, Ting Song
wiley   +1 more source

The Role of Post-translational Modifications on the Energy Landscape of Huntingtin N-Terminus

open access: yesFrontiers in Molecular Biosciences, 2019
Huntington disease is a neurodegenerative disease characterized by a polymorphic tract of polyglutamine repeats in exon 1 of the huntingtin protein, which is thought to be responsible for protein aggregation and neuronal death. The polyglutamine tract is
Havva Yalinca   +6 more
doaj   +1 more source

Huntington\u27s Disease--A Review [PDF]

open access: yes, 2016
Huntington’s disease is degenerative and effects both cognitive and motor functioning, beginning in the 20s and continuing a decline for about two decades until death.
Dunn, Christen
core   +1 more source

Lipid composition controls the huntingtin exon 1 membrane‐association and differentially modulates its flanking regions' dynamics

open access: yesProtein Science, Volume 35, Issue 6, June 2026.
Abstract The pathological expansion of the polyglutamine (polyQ) repeat within the first exon of huntingtin (Httex1) protein is a defining hallmark of Huntington's disease (HD). Multiple evidence supports that the membrane recruitment of Httex1 is critical for its self‐assembly and related toxicity in HD.
Tânia Sousa   +6 more
wiley   +1 more source

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